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Final Flashcards

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1
Q

What is azotemia?

A

an accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood

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2
Q

What is urea? How is it measured? What is the normal value?

A

BUN

By product of protein

=20

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3
Q

What is creatinine? How is it measured? What is the normal value?

A

By product of muscle

=1

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4
Q

What are waste products?

A

Urea
Creatinine
Electrolytes

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5
Q

Acute Kidney Injury (AKI) stage 1

A

Prerenal = decreased blood flow, decreased blood volume

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6
Q

Prerenal causes of AKI

A

Hypovolemia
Decreased cardiac output
Decreased vascular resistance
Decreased renovascular blood flow

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7
Q

Hypovolemia (prerenal) causes

A
  • dehydration
  • hemorrhage
  • GI losses (diarrhea, vomiting)
  • excessive diuresis
  • hypoalbuminemia
  • burns
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8
Q

Decreased CO (prerenal) causes

A
  • dysrhythmias
  • cardiogenic shock
  • heart failure
  • MI
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9
Q

Decreased vascular resistance (prerenal) causes

A
  • anaphylaxis
  • neuro injury
  • septic shock
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10
Q

Decreased renovascular blood flow (prerenal) causes

A
  • bilateral renal vein thrombosis
  • embolism
  • hepatorenal syndrome
  • renal artery thrombosis
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11
Q

Acute Kidney Injury (AKI) stage 2

A

Intrarenal = inside the kidney

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12
Q

Intrarenal causes

A

Nephrotoxic injury
Interstitial nephritis
Other causes

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13
Q

Nephrotoxic injury (intrarenal) causes

A
  • drugs: aminoglycosides (gentamicin), amphotericin B
  • contrast media
  • hemolytic blood transfusion reaction
  • severe crush injury
  • chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride
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14
Q

Interstitial nephritis (intrarenal) causes

A
  • allergies: antibiotics (sulfonamides, rifampin), NSAIDS, ACE inhibitors
  • infections: bacterial (acute pyelonephritis), viral (CMV), funal (candidiasis)
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15
Q

Other causes of intrarenal

A
  • prolonged prerenal ischemia
  • acute glomerulonephritis
  • thrombotic disorders
  • toxemia of pregnancy
  • malignant hypertension
  • systemic lupus erythematosus
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16
Q

Acute Kidney Injury (AKI) stage 3

A

Postrenal = blockage in kidney! (back up of urine)

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17
Q

Postrenal causes

A
  • BPH
  • bladder or prostate cancer
  • calculi formation
  • neuromuscular disorders
  • spinal cord disease
  • strictures
  • trauma (back, pelvis, perineum)
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18
Q

AKI phases

A

Oliguric or nonoliguric
Diuretic
Recovery

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19
Q

Oliguric phase of AKI

A

*holding onto waste

  • decreased urine output <400 mL/day
  • hypervolemia
  • edema in extremities
  • hypertension
  • pulmonary edema, crackles, short of breath
  • metabolic acidosis
  • increased BUN, creatinine, K
  • decreased Na

*asterixis-flapping hand motion

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20
Q

Nonoliguric phase of AKI

A

urine output >400 mL/day

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21
Q

What should be restricted during oliguric phase?

A

Potassium
Sodium
Protein

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22
Q

If protein is low, give _______.

A

albumin

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23
Q

Diuretic phase of AKI

A

(hypo everything!)

  • urine output 5L/day
  • hypovolemia
  • hyponatremia
  • hypotension
  • hypokalemia
  • dehydration
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24
Q

Recovery phase of AKI

A
  • GFR increases
  • BUN and creatinine decrease
  • casts-tubules sloughing
  • dark, concentrated urine

*high protein and calorie diet

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25
Normal GFR
125 mL/min
26
GFR ________ with injury
decreases
27
GFR ________ when recovery phase begins in AKI
increases
28
Chronic Kidney Disease (CKD) is...
progressive and irreversible
29
CKD manifestations | Psychologic
- anxiety | - depression
30
CKD manifestations | Cardio
- HTN - HF - CAD - pericarditis - PAD
31
CKD manifestations | GI
- anorexia - N/V - GI bleeding - gastritis
32
CKD manifestations | Endocrine
- hyperparathyroidism - amenorrhea - erectile dysfunction - thyroid abnormalities
33
CKD manifestations | Metabolic
- carb intolerance | - hyperlipidemia
34
CKD manifestations | Hematologic
- anemia - bleeding - infection
35
CKD manifestations | Neuro
- fatigue - headache - sleep disturbances - encephalopathy
36
CKD manifestations | Ocular
-hypertensive retinopathy
37
CKD manifestations | Pulmonary
- pulmonary edema - uremic pleuritis - pneumonia
38
CKD manifestations | Integumentary
- pruritis - ecchymosis - dry, scaly skin
39
CKD manifestations | Musculoskeletal
- vascular and soft tissue calcifications - osteomalacia - osteitis fibrosa
40
CKD manifestations | Peripheral neuropathy
- parathesias | - RLS
41
Stage 1 of CKD
GFR >90 manage with diet control B/P
42
Stage 2 of CKD
GFR 60-89 manage with diet control B/P
43
Stage 3 of CKD
GFR 30-59
44
Stage 4 of CKD
GFR 15-29
45
Stage 5 of CKD
GFR <15 Kidney failure
46
Chronic Renal Failure (CRF)
-diminished renal reserve (stages 1 and 2 of CKD) -renal insufficiency (stages 3 and 4 of CKD) -end stage renal disease (ESRD) (stage 5 of CKD)
47
Diminished renal reserve | stages 1 and 2 of CKD
- GFR >90 mL/min - control B/P - kidney damage with normal or increased GFR - decreased urinary concentration (nocturia) - treatment of diabetes, hypertension, renal artery stenosis - 24 hour urine (creatinine)
48
Renal insufficiency | stages 3 and 4 of CKD
- GFR 30-89 mL/min - headaches - decreased ability to concentrate urine - polyuria to oliguria - increased BUN, creatinine - edema - mild anemia - increased B/P - weakness/fatigue
49
End stage renal disease (ESRD) | stage 5 of CKD
- GFR <15 mL/min - confusion, weakness, fatigue - increased B/P, pitting edema, increased CVP, pericarditis - SOB, suppressed cough, thick sputum - amonia odor to breath, metallic taste, mouth ulcers, anorexia, N/V - behavior changes - anemia (decreased RBC, increased HR) - dry, flaky skin, pruritis, ecchymosis, pupura - cramps, renal osteodystrophy, bone pain
50
Diffusion
urea, creatinine, uric acid and electrolytes move from the blood to the dialysate to lower the concentration in the blood
51
Osmosis
glucose is added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood
52
Advantages of peritoneal dialysis (PD)
- immediate initation in most hospitals - less complicated - portable system with CAPD - fewer dietary restrictions - pts with vascular access problems - decreased cardio stress - home dialysis possible - preferable for diabetes pt
53
Advantages of hemodialysis (HD)
- rapid fluid removal - rapid urea and creatinine removal - potassium removal - less protein loss - decreased triglycerides - temporary access can be placed at bedside
54
Process for PD
Exchange | 3 phases
55
Phase 1 of PD
Inflow -2L solution infuses-10 minutes
56
Phase 2 of PD
Dwell - diffusion and osmosis between pt's blood and peritoneal cavity - 20 or 30 min-8 hours, depending on method
57
Phase 3 of PD
Drain - 15-30 minutes - can be facilitated by gently massaging abdomen or changing position
58
Process for HD
1 needle pulls blood | 1 needle puts blood back into pt
59
Potential complications of PD
- infections - pain - peritonitis - heart problems - pulmonary problems (pneumonia, atelectasis, bronchitis) - protein loss - carb abnormalities
60
Potential complications of HD
- hypotension - muscle cramps - hepatitis - infection - heart disease
61
Human Leukocyte Antigen (HLA)
- antigens responsible for rejection of genetically unlike tissue - histocompatibility antigens - matching organs and tissues for transplants
62
The more HLA matches =
less likely for rejection
63
HLA matching for corneas
None needed (avascular)
64
HLA matching for liver, heart, lungs
some needed
65
HLA matching for kidneys and bone marrow
EXACT match needed
66
Positive crossmatch
bad reaction with donor/recipient blood
67
Negative crossmatch
NO reaction | -organ safe for transplantation
68
What tests are needed for transplants?
HLA matching Crossmatch ABO
69
Types of rejection
- hyperacute - acute - chronic
70
Hyperacute rejection
- within 24 hours - blood vessels destroyed rapidly from pre-existing antibodies (positive crossmatch) - RARE - No treatment - transplant organ needs to be removed
71
Acute rejection
- within 6 months - recipients lymphocytes activated against donated tissue or antibodies develop after transplant - common with deceased organs - REVERSIBLE-treat with immunosuppressants and corticosteroids
72
Chronic rejection
- over months or years - repeated acute rejections - fibrosis and scarring occurs - IRREVERSIBLE-pt placed on transplant list - difficult to manage, support therapy needed
73
Graft vs host disease
occurs when immuno-incompetent pt transfused or transplanted with immuno-competent cells *donor T cells attack recipient
74
Graft vs host disease manifestations | ONLY 3
Skin-maculopapular rash to desquamation Liver-mild jaundice to hepatic coma GI-diarrhea, GI bleeding, malabsorption, abdominal pain
75
PCs for organ transplantation
- rejection - susceptibility to infection - heart disease - malignancies - recurrence of kidney disease - corticosteroid-related complications
76
Determines how well pt is oxygenated
PaO2
77
Determines how well pt is ventilating
PaCO2
78
3 mechanisms that control acid/base
Kidney-bicarb (HCO3) Lungs-carbon dioxide (CO2) Buffer-electrolytes
79
Normal pH range
7.35-7.45
80
Normal range for PaCO2
35-45
81
Normal range for HCO3
22-26
82
ABG sites
- radial artery (most common) - brachial artery (avoid in obese pts) - femoral artery (only used as last resort)
83
When doing the Allen's test, which artery do you release pressure?
ULNAR ARTERY!
84
Blood will _______ into the syringe
pulsate
85
Blood gas syringes fill by themselves, stopping at ___
2mL
86
Indications for arterial lines
- Frequent ABG sampling | - Continuous BP monitoring
87
Indications for continuous BP monitoring
- shock - infusion of vasoactive drugs - procedures for coronary interventions - acute hypo and hypertension - respiratory failure - neuro injuries
88
How often should ABG draws be done if pt is on a vent?
Daily AM
89
Arterial line complications
- hemorrhage - infection - thrombus formation - neuro impairment - loss of limb
90
True or false: H+, CO2, and K is more acidic
TRUE
91
Acidosis indicates an ______ of H+, and a _______ of HCO3
excess; deficit
92
Alkalosis indicates an ______ of HCO3, and a ______ of H+
excess; deficit
93
pH <7.35
acidosis
94
pH >7.45
alkalosis
95
What does high PaCO2 indicate?
Respiratory acidosis
96
What does low PaCO2 indicate?
Respiratory alkalosis
97
What does high HCO3 indicate?
Metabolic alkalosis
98
What does low HCO3 indicate?
Metabolic acidosis
99
Respiratory acidosis causes
(Hypoventilation) - COPD - OD/sedation - chest trauma - severe pneumonia - pulmonary edema - atelectasis - respiratory muscle weakness - mechanical hypoventilation * phrenic nerve injury (C2)
100
Respiratory alkalosis causes
- hyperventilation - stimulated respiratory center - mechanical hyperventilation
101
Respiratory alkalosis hyperventilation causes
- hypoxia - PE - anxiety - fear - pain - exercise - fever - high altitudes - pregnancy
102
Respiratory alkalosis stimulated respiratory center causes
- septicemia - encephalitis - brain injury - salicylate poisoning
103
Metabolic acidosis causes
- DKA - diarrhea - renal failure - shock - salicylate OD - sepsis
104
Metabolic alkalosis causes
- loss of gastric secretions (NG suction, severe vomiting) - diuretic therapy (K wasting diuretics) - overuse of antacids
105
Normal intracranial pressure (ICP)
5-15 mmHg
106
Normal compensatory adaptations
- changes in CSF volume | - cerebral vasodilation or vasoconstriction
107
Cerebrospinal fluid =
10%
108
Intravascular blood =
12%
109
Brain tissue =
78%
110
Autoregulation of cerebral blood flow (CBF)
- brain has ability to regulate own blood flow - ensures adequate blood flow to brain - influenced by systemic arterial pressure
111
How much glucose and O2 does brain need?
25% and 20%
112
Cerebral perfusion pressure (CPP)
pressure needed to ensure blood flow to brain
113
Normal CPP
60-100 mmHg
114
How to calculate CPP
MAP-ICP=CPP
115
CPP <50 mmHg
associated with ischemia and neuronal death`
116
Compliance
expandibility of the brain
117
Stage 1 of CBF
- high compliance - increase of volume in brain does not increase ICP - autoregulation intact
118
Stage 2 of CBF
- compliance lessens | - increase of volume in brain increases risk of increasing ICP
119
Stage 3 of CBF
- decrease compliance - small addition of volume increases ICP - loss of autoregulation - B/P rises to maintain CPP - decompensation about to happen * cushing's triad
120
Stage 4 of CBF
- ICP at lethal levels with little increase in volume | - herniation of brain
121
Cushing's triad
EMERGENCY!!! - systolic HTN with widening pulse pressure - bradycardia with full and bounding pulse - altered respirations
122
Types of brain herniation
- tentorial herniation - uncal herniation - cingulate herniation
123
Tentorial herniation
herniation downward through the brainstem opening
124
Uncal herniation
lateral and downward
125
Cingulate herniation
lateral, beneath the falx cerebri
126
High CO2 in the brain =
cerebral vessels to dilate = increases CBF
127
Low CO2 in the brain =
cerebral vessels to constrict = decreases CBF
128
Low levels of O2 in brain =
cerebral dilation = increases CBF
129
Most sensitive indicator for evaluating pt's neuro status
Level of consciousness (LOC)
130
Cranial nerve III
oculomotor nerve
131
What happens if CN III is compressed?
- dilation of pupil on same side (ipsilateral) as lesion - sluggish or no response to light - inability to move eye upward - ptosis of eyelid
132
Decorticate posturing
internal rotation and adduction of arms with flexion of elbows, wrists and fingers.
133
Why does decorticate posturing happen?
there's an interruption of voluntary motor tracts in cerebral cortex
134
Decerebrate posturing
- arms stiffly extended, abducted, and hyperpronated | - hyperextension of legs with plantar flexion of feet
135
Why does decerebrate posturing happen?
there's a disruption of motor fibers in midbrain and brainstem
136
Is decorticate or decerebrate posturing more serious?
decerebrate posturing
137
What is the halo sign test?
to determine if drainage from ear or nose is CSF -drip onto gauze, if yellow ring encircles the blood, CSF is present
138
Interventions for pt with ICP
- nutritional therapy - respiratory function - fluid/electrolyte balance - monitor ICP - semi-fowler's position - protection from injuries (high risk for seizures)
139
Drug therapy for pt with ICP
- mannitol-pulls fluid from brain into bloodstream (rises B/P - hypertonic solution (NS 3%-same outcome as mannitol) - vasopressors-rise B/P - corticosteroids (if pt doesn't have head injury) - prophylactic seizure meds
140
3 areas assess for Glascow Coma Scale (GCS)
- open eyes - best verbal response - best motor response
141
Purpose of GCS
to assess LOC of pt
142
Nutritional therapy for pt with ICP
- increase glucose as needed - nutrition replacement within 3 days of injury - malnutrition promotes continued cerebral edema
143
GCS of __ generally indicates coma
<8
144
Head injury is any trauma to the...
- skull - scalp - brain
145
GCS-eyes open score spontaneous response to bedside approach, pain, or verbal command
4
146
GCS-eyes open score opening eyes to name or command
3
147
GCS-eyes open score lack of opening eyes to name or command, but open to pain
2
148
GCS-eyes open score lack of opening of eyes to stimuli
1
149
GCS-eyes open score untestable
U
150
GCS-best verbal response score A&O x4
5
151
GCS-best verbal response score confusion, conversant, but disoriented
4
152
GCS-best verbal response score inappropriate or disorganized use of words, lack of sustained conversation
3
153
GCS-best verbal response score incomprehensible words, sounds (moaning)
2
154
GCS-best verbal response score lack of sound, even with painful stimuli
1
155
GCS-best verbal response score untestable
U
156
GCS-best motor response score Obedience of verbal command (raise arm, hold up 2 fingers)
6
157
GCS-best motor response score localization of pain, lack of obedience but makes attempts to remove painful stimulus (pressure on nail)
5
158
GCS-best motor response score arm flexion withdrawal
4
159
GCS-best motor response score abnormal flexion-flexion of arm at elbow and pronation, making a fist
3
160
GCS-best motor response score abnormal extension of arm at elbow usually with adduction and internal rotation of arm at shoulder
2
161
GCS-best motor response score lack of response
1
162
GCS-best motor response score untestable
U
163
Linear skull fracture
straight
164
Depressed skull fracture
broke down
165
Comminuted skull fracture
pieces
166
Battle's sign
bruising on eyes and ears
167
True or false Blood has glucose
TRUE
168
Contusion
bruising of brain tissue
169
Coup-contrecoup injury
bruising on 2 parts of brain due to brain shifting and hitting against skull
170
Epidural hematoma
- bleeding between dura and inner surface of skull - venous or arterial origin - neuro emergency if arterial!
171
Subdural hematoma
- bleeding between dura mater and arachnoid layer of meninges - usually venous - results from injury to brain tissue and its blood vessels
172
Acute subdural hematoma
24-48 hours after injury
173
Subacute subdural hematoma
48 hours-2 weeks after injury
174
Chronic subdural hematoma
weeks to months after injury (usually >20 days)
175
Intracerebral hematoma
- bleeding within brain tissue - in approx. 16% of head injuries - usually occurs within frontal and temporal lobes, possible from rupture of vessels at time of injury - size and location determines pt outcome
176
Burr hole
opening into cranium with drill to remove fluid and blood beneath dura
177
Craniotomy
removal of bone flap to remove lesion, repair a damaged area, drain blood or relieve increased ICP
178
Craniectomy
incision into cranium to cut away bone flap
179
Ventricolostomy
- directly measures pressure within the ventricles - facilitates removal and/or sampling of CSF - allows for intraventricular drug administration
180
Non-modifiable risk factors for stroke
- age - gender - ethnicity or race - family history - heredity
181
Modifiable risk factors for stroke
- HTN - heart disease - diabetes mellitus - smoking - excessive alcohol consumption - obesity - sleep apnea - metabolic syndrome - lack of exercise - poor diet - drug abuse
182
When blood flow to the brain is completely interrupted, neuro metabolism is altered in __ seconds.
30
183
When blood flow to the brain is completely interrupted, metabolism stops in __ minutes.
2
184
When blood flow to the brain is completely interrupted, cell death occurs in __ minutes
5
185
Transient ischemic attacks (TIA)
- temporary loss of neuro function - most resolve within 3 hours - leads up to a stroke
186
Classification of strokes
- ischemic | - hemorrhagic
187
Types of ischemic strokes
- thrombotic | - embolic
188
Ischemic=
lack of O2
189
Thrombotic stroke
MOST COMMON - injury to or narrowing of a blood vessel wall - formation of blood clot
190
Embolic stroke
- embolus occludes cerebral artery | - infarction and edema of area
191
Types of hemorrhagic strokes
- intracerebral hemorrhage | - subarachnoid hemorrhage
192
Intracerebral hemorrhage
- bleeding within the brain caused by rupture of a vessel | - HTN is the most important cause
193
Subarachnoid hemorrhage
- intracerebral bleeding into CSF-filled space between arachnoid and pia mater - commonly caused by rupture of cerebral aneurysm
194
Sign of subarachnoid hemorrhage
"worst headache of one's life"
195
Receptive dysphasia
doesn't understand what was said
196
Expressive aphasia
understood but can't express feeling
197
Right-brain damage
Effects left side of body "I'm right" Safety!
198
Left-brain damage
Effects right side of body Language
199
Lack of nutrition leads to edema where?
brain
200
CT should be obtained within __ minutes and read within __ minutes of ER arrival
25; 45
201
Purpose of CT with stroke
- indicate size and location of lesion - determine if ischemic or hemorrhagic *NO contrast
202
Stroke pt should be doing what type of ROM daily
passive
203
First things to do for stroke pt
- CT scan - NG - foley
204
tPA
- re-establish blood flow | - must be administered within 3 hours of onset of symptoms
205
tPA IV
- monitor VS q15min - ANY hint of bleeding: STOP! - hang saline
206
Possible treatment for strokes
- clipping | - coiling
207
CANNOT RECEIVE tPA
- clotting disorder - hemorrhagic stroke - active bleed - neoplasm=cancer
208
Number of cervical vertebrae
7
209
Number of thoracic vertebrae
12
210
Number of thoracic vertebrae
5
211
C5 =
phrenic nerve "C5 keeps the diaphragm alive"
212
Spinal shock
- decrease reflexes - loss of sensation - flaccid paralysis below level of injury
213
Treatment for spinal shock
supportive care
214
Neurogenic shock
(cardiac effects) - loss of vasomotor tone (vasodilation) - hypotension & bradycardia - associated with T6 injury of higher
215
Neurogenic shock treatment
- atropine | - vasopressors
216
Tetraplegia is the same as
quadraplegia
217
C7-T1 injury =
tetraplegia
218
T1 and below injury =
paraplegia
219
T5 =
upper GI
220
T6 =
cardiac
221
T10 =
GU
222
T2 =
lower GI
223
Neurogenic shock causes a decrease in __ and __
B/P and HR
224
Complete cord involvement
total loss of sensory and motor function below level of injury
225
Incomplete (partial) cord involvement
mixed loss of voluntary motor activity and sensation *some tracts intact
226
Higher the injury =
more serious
227
C5 and above injury
total loss of respiratory muscle function
228
What is required with C5 and above injury?
mechanical ventilation
229
C5 and below injury
- diaphragmatic breathing | - hypoventilation if phrenic nerve is functioning
230
Cervical and thoracic injuries cause paralysis of
- abdominal muscles | - intercostal muscles
231
Pt cannot cough effectively with cervical and thoracic injuries, leading to
atelectasis or pneumonia
232
Acute
first 48-72 hours
233
Any cord injury above level T6 =
neurogenic shock
234
T6 and above injury
- bradycardia - hypotension - relative hypovolemia exists because of increase in venous capacitance
235
T10 and below injury
- urinary retention | - bladder-atonic & distended, hyperirritable
236
What is needed with T10 and below injury?
indwelling catheter *increases risk for infection
237
T5 and above injury
hypomotility - paralytic ileus - gastric distention - stress ulcers - intraabdominal bleeding may occur
238
T5 and above injury nursing
- NG placement - monitor for distended abdomen - increased for aspiration - give PPIs
239
Injury of T12 or below
neurogenic bowel - bowel is areflexic - decreased sphincter tone - constipation
240
Injury of T12 or below nursing
- dig stim, colace, fiber - bowel training - mineral oil
241
Poikilothermism
adjustment of body temp to room temp
242
True or False Surgery is only done when there's cord compression
True
243
NGT suctioning can lead to
metabolic alkalosis
244
Decreased tissue perfusion (shock) leads to
metabolic acidosis
245
High risk population for spinal cord injuries
Teens and young males
246
Bones heal in
6-8 weeks
247
Cervical traction is used to
- decrease inflammation | - promote healing
248
Autonomic dysreflexia
Life threatening cardio reaction by SNS
249
Cause of autonomic dysreflexia
- distended bladder or rectum - tight clothing - anything that causes pain
250
S/S of autonomic dysreflexia
- severe HTN - blurred vision - throbbing headache - diaphoresis (above level of injury) - bradycardia - piloerection (hairs on skin) - skin flushing - anxiety
251
Goal for autonomic dysreflexia
Get B/P down!!!
252
Nursing interventions for autonomic dysreflexia
1. elevate HOB 45 degrees, or sit pt upright 2. assess cause 3. catheterization 4. notify physician
253
Acute Respiratory Failure (ARF)
-results from inadequate gas exchange
254
insufficient O2 transferred to the blood
hypoxemia (decreased O2)
255
Inadequate CO2 removal
hypercapnic (increased CO2)
256
Adequate PaO2
80-100
257
Hypoxemia is what type of failure
oxygenation
258
Hypercapnic is what type of failure
ventilation
259
Causes of hypoxemic respiratory failure
- V/Q mismatch - shunt - diffusion limitation - alveolar hypoventilation
260
V/Q mismatch causes
- pneumonia - atelectasis - pulmonary embolus
261
Gas exchangeis better in what part of the lungs?
base of lungs
262
What is shunting?
blood exits the heart without gas exchange
263
Types of shunts
Anatomic shunt | Intrapulmonary shunt
264
What is an anatomic shunt?
heart defect-bypass lungs
265
What is an intrapulmonary shunt?
inside lungs-NO gas exchange
266
CO2 retention results in...
hypoxemia
267
What percentage of O2 is in room air?
21%
268
Percentage of O2 in 1L
3-4%
269
More CO2 retained, causes pH to...
decrease
270
Ventilation is ....
breathing (lung and heart)
271
Perfusion is ....
blood flow (gas exchange)
272
Ratio of inhale and exhale
1:2
273
Diffusion limitation
thickened membranes (scar tissue)
274
Examples of diffusion limitation
- severe emphysema - pulmonary fibrosis - ARDS
275
Alveolar hypoventilation
decrease in ventilation -increase PaCO2, decrease in PaO2
276
Atelectasis
alveolar collapse, resulting in NO gas exchange
277
Primary cause of alveolar hypotension
hypercapnic respiratory failure
278
Hypercapnic respiratory failure
inability to remove sufficient CO2 to maintain normal PaO2
279
Causes of hypercapnic respiratory failure
- airway and alveoli (respiratory) - CNS - chest wall - neuro conditions
280
The ONLY 3 respiratory issues that are related to hypercapnic
- COPD - Asthma - Cystic Fibrosis
281
True or False: CO2 in the brain is a vasoconstricter
FALSE CO2 is a vasodilator
282
Early signs of respiratory failure
- restlessness, confusion - tachycardia - tachypnea - mild HTN
283
Late sign of respiratory failure
cyanosis
284
Consequences of hypoxemia and hypoxia
- metabolic acidosis and cell death - decreased CO - impaired renal function (decreased B/P)
285
What are ways to prevent of acute respiratory failure?
- early recognition of respiratory distress | - flu or pneumo vax (elderly, diabetics, anyone with low immune system)
286
O2 toxicity can cause what?
atelectasis
287
Positive-pressure ventilation (PPV)
intubation
288
Examples non invasive PPV
Bi-PAP | CPAP
289
Bi-PAP
inhalation and exhalation
290
CPAP
continuous positive airway pressure inhalation
291
What physiologic changes in the respiratory system happen in aging?
- decreased ventilatory capacity - alveolar dilation - larger air spaces - loss of surface area - diminished elastic recoil - decreased respiratory muscle strength - decreased chest wall compliance
292
What is Acute Respiratory Distress Syndrome (ARDS)?
widespread **INFLAMMATION** - increased neutrophils (WBC-line alveoli membrane) - increased pulmonary capillary permeability
293
Phases of ARDS
- injury or exudative - reparative or proliferative - fibrotic
294
What does an ARDS chest x ray look like?
Bilateral pulmonary infiltrates
295
Injury or exudative phase of ARDS
- pulmonary edema - surfactant (keeps alveoli open) doesn't work anymore or body stops production, causing atelectasis - scar tissue from damage to alveoli becomes thick
296
ARDS is what type of respiratory failure
hypoxemic
297
Reparative or proliferative phase ARDS
pt gets better or gets worse
298
Fibrotic phase ARDS
the alveoli scar tissue becomes worse and stiff = NO gas exchange *permanent damage, will most likely die
299
What is mortality rate for pt's with ARDS?
50%
300
What is FiO2?
Amount of O2 pt is on
301
What is PEEP on ventilator?
Positive End Expectory Pressure -pops alveoli open
302
What gets O2 directly into lungs?
ET tube
Role and scope
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